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Review Article
Mechanisms of Vascular Calcification: The Pivotal Role of Pyruvate Dehydrogenase Kinase 4
Jaechan Leem, In-Kyu Lee
Endocrinol Metab. 2016;31(1):52-61.   Published online March 16, 2016
DOI: https://doi.org/10.3803/EnM.2016.31.1.52
  • 5,278 View
  • 73 Download
  • 30 Web of Science
  • 28 Crossref
AbstractAbstract PDFPubReader   

Vascular calcification, abnormal mineralization of the vessel wall, is frequently associated with aging, atherosclerosis, diabetes mellitus, and chronic kidney disease. Vascular calcification is a key risk factor for many adverse clinical outcomes, including ischemic cardiac events and subsequent cardiovascular mortality. Vascular calcification was long considered to be a passive degenerative process, but it is now recognized as an active and highly regulated process similar to bone formation. However, despite numerous studies on the pathogenesis of vascular calcification, the mechanisms driving this process remain poorly understood. Pyruvate dehydrogenase kinases (PDKs) play an important role in the regulation of cellular metabolism and mitochondrial function. Recent studies show that PDK4 is an attractive therapeutic target for the treatment of various metabolic diseases. In this review, we summarize our current knowledge regarding the mechanisms of vascular calcification and describe the role of PDK4 in the osteogenic differentiation of vascular smooth muscle cells and development of vascular calcification. Further studies aimed at understanding the molecular mechanisms of vascular calcification will be critical for the development of novel therapeutic strategies.

Citations

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  • Gamut of glycolytic enzymes in vascular smooth muscle cell proliferation: Implications for vascular proliferative diseases
    Ankan Sarkar, Sandip V. Pawar, Kanwaljit Chopra, Manish Jain
    Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease.2024; 1870(3): 167021.     CrossRef
  • MAPK14 as a key gene for regulating inflammatory response and macrophage M1 polarization induced by ferroptotic keratinocyte in psoriasis
    Lin Zhou, Yingdong Zhong, Chaowei Li, Yu Zhou, Xi Liu, Lincai Li, Zhengwei Zou, Zhihui Zhong, Junsong Ye
    Inflammation.2024;[Epub]     CrossRef
  • Pyruvate dehydrogenase kinase 4 promotes osteoblastic potential of BMP9 by boosting Wnt/β-catenin signaling in mesenchymal stem cells
    Yuan-Yuan Yang, Hong-Hong Luo, Yi-Xuan Deng, Xin-Tong Yao, Jie Zhang, Yu-Xi Su, Bai-Cheng He
    The International Journal of Biochemistry & Cell Biology.2023; 154: 106341.     CrossRef
  • lncRNA MEG3 Promotes PDK4/GSK-3β/β-Catenin Axis in MEFs by Targeting miR-532-5p
    Yuan-Yuan Yang, Yi-Xuan Deng, Xin-Tong Yao, Hong-Hong Luo, Wen-Ge He, Xuan-Ling Cao, Rong-Chun Chen, Bai-Cheng He, Hai-Tao Jiang, Jing Wang, Sedat Kacar
    Oxidative Medicine and Cellular Longevity.2023; 2023: 1.     CrossRef
  • Mitochondrial dynamics in vascular remodeling and target-organ damage
    Tong Zhu, Qingxun Hu, Yanggang Yuan, Huijuan Yao, Jian Zhang, Jia Qi
    Frontiers in Cardiovascular Medicine.2023;[Epub]     CrossRef
  • PDK4-dependent hypercatabolism and lactate production of senescent cells promotes cancer malignancy
    Xuefeng Dou, Qiang Fu, Qilai Long, Shuning Liu, Yejun Zou, Da Fu, Qixia Xu, Zhirui Jiang, Xiaohui Ren, Guilong Zhang, Xiaoling Wei, Qingfeng Li, Judith Campisi, Yuzheng Zhao, Yu Sun
    Nature Metabolism.2023; 5(11): 1887.     CrossRef
  • Identification of PDK4 as Hub Gene for Diabetic Nephropathy Using Co-Expression Network Analysis
    Yuanyuan Han, Liangzi Jin, Liangzhi Wang, Lan Wei, Chao Tu
    Kidney and Blood Pressure Research.2023; 48(1): 522.     CrossRef
  • Flavocoxid Ameliorates Aortic Calcification Induced by Hypervitaminosis D3 and Nicotine in Rats Via Targeting TNF-α, IL-1β, iNOS, and Osteogenic Runx2
    Ahmed E. Amer, George S. G. Shehatou, Hassan A. El-Kashef, Manar A. Nader, Ahmed R. El-Sheakh
    Cardiovascular Drugs and Therapy.2022; 36(6): 1047.     CrossRef
  • Diabetic mellitus, vascular calcification and hypoxia: A complex and neglected tripartite relationship
    Xue-Jiao Sun, Nai-Feng Liu
    Cellular Signalling.2022; 91: 110219.     CrossRef
  • Insights Into the Role of Mitochondria in Vascular Calcification
    ZL Zeng, Qing Yuan, Xuyu Zu, Jianghua Liu
    Frontiers in Cardiovascular Medicine.2022;[Epub]     CrossRef
  • Induced pluripotent stem cell-derived smooth muscle cells to study cardiovascular calcification
    Samantha K. Atkins, Abhijeet R. Sonawane, Romi Brouwhuis, Johana Barrientos, Anna Ha, Maximillian Rogers, Takeshi Tanaka, Takehito Okui, Shiori Kuraoka, Sasha A. Singh, Masanori Aikawa, Elena Aikawa
    Frontiers in Cardiovascular Medicine.2022;[Epub]     CrossRef
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    Frontiers in Cardiovascular Medicine.2022;[Epub]     CrossRef
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    Ishita Tandon, Kyle P. Quinn, Kartik Balachandran
    Frontiers in Cardiovascular Medicine.2021;[Epub]     CrossRef
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    Sun Joo Lee, In-Kyu Lee, Jae-Han Jeon
    International Journal of Molecular Sciences.2020; 21(8): 2685.     CrossRef
  • Osteocalcin Regulates Arterial Calcification Via Altered Wnt Signaling and Glucose Metabolism
    Nabil A Rashdan, Alisia M Sim, Lin Cui, Kanchan Phadwal, Fiona L Roberts, Roderick Carter, Derya D Ozdemir, Peter Hohenstein, John Hung, Jakub Kaczynski, David E Newby, Andrew H Baker, Gerard Karsenty, Nicholas M Morton, Vicky E MacRae
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    Journal of Translational Internal Medicine.2020; 8(2): 80.     CrossRef
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    Peter Stoeter, Pedro Roa-Sanchez, Cesar F Gonzalez, Herwin Speckter, Jairo Oviedo, Pamela Bido
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  • PDK4 promotes vascular calcification by interfering with autophagic activity and metabolic reprogramming
    Wen-Qi Ma, Xue-Jiao Sun, Yi Zhu, Nai-Feng Liu
    Cell Death & Disease.2020;[Epub]     CrossRef
  • Restoring mitochondrial biogenesis with metformin attenuates β-GP-induced phenotypic transformation of VSMCs into an osteogenic phenotype via inhibition of PDK4/oxidative stress-mediated apoptosis
    Wen-Qi Ma, Xue-Jiao Sun, Ying Wang, Yi Zhu, Xi-Qiong Han, Nai-Feng Liu
    Molecular and Cellular Endocrinology.2019; 479: 39.     CrossRef
  • Salusin-β Promotes Vascular Calcification via Nicotinamide Adenine Dinucleotide Phosphate/Reactive Oxygen Species-Mediated Klotho Downregulation
    Haijian Sun, Feng Zhang, Yu Xu, Shuo Sun, Huiping Wang, Qiong Du, Chenxin Gu, Stephen M. Black, Ying Han, Haiyang Tang
    Antioxidants & Redox Signaling.2019; 31(18): 1352.     CrossRef
  • Fibroblast Growth Factor 21 (FGF21) Promotes Formation of Aerobic Myofibers via the FGF21‐SIRT1‐AMPK‐PGC1α Pathway
    Xinyi Liu, Yongliang Wang, Liming Hou, Yuanzhu Xiong, Shuhong Zhao
    Journal of Cellular Physiology.2017; 232(7): 1893.     CrossRef
  • Articles inEndocrinology and Metabolismin 2016
    Won-Young Lee
    Endocrinology and Metabolism.2017; 32(1): 62.     CrossRef
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Original Articles
The Effect of Epicatechin on the High Glucose-induced TSP-1 Expression and MMP-2 Activity in Rat Vascular Smooth Muscle Cells.
Gyeong Ryul Ryu, Jung Hoon Kang, Kyong Ja Hong, In Kyung Jeong, Hwa In Jang, Duck Joo Rhie, Shin Hee Yoon, Sang June Hahn, Myung Suk Kim, Yang Hyeok Jo, Myung Jun Kim
J Korean Endocr Soc. 2006;21(4):302-310.   Published online August 1, 2006
DOI: https://doi.org/10.3803/jkes.2006.21.4.302
  • 2,113 View
  • 31 Download
  • 1 Crossref
AbstractAbstract PDF
BACKGROUND
The incidence of atherosclerosis is well correlated with the progression of type 2 diabetes mellitus. High plasma glucose in uncontrolled diabetic patients evokes many vascular complications such as atherosclerosis. Specifically, high glucose was reported to induce thrombospondin-1 (TSP-1), which activates matrix metalloproteinase-2 (MMP-2) and leads to the invasion of vascular smooth muscle cells (VSMCs) into the intima. Catechins with antioxidant effects are known to inhibit MMP-2 activity. Therefore, this study was aimed at revealing the effect of epicatechin, one of catechins, on high glucose-induced TSP-1 and the invasiveness of VSMCs. METHODS: VSMCs were primarily isolated from Sprague-Dawley rat aorta. The VSMCs were incubated with different doses (30, 100 and 300 micrometer) of epicatechin under high glucose concentration (30 mM). The TSP-1 protein and mRNA expressions were analyzed by performing Western blotting and Northern blot analyses, respectively. RT-PCR was performed to observe the MMP-2 mRNA expression. Gelatin zymography was performed for the measurement of MMP-2 activity. Invasion assays were performed to evaluate the invasiveness of VSMCs. RESULTS: Epicatechin inhibited the high glucose-induced TSP-1 expression and the MMP-2 activity in a dose-dependent manner. Also, epicatechin inhibited the high glucose-induced invasiveness of VSMCs across the matrix barrier in a dose-dependent fashion. CONCLUSION: Collectively, epicatechin may prevent the high glucose-induced proliferation and invasion of VSMCs by inhibiting the TSP-1 expression and the MMP-2 activity. Therefore, epicatechin appears to play a protective role in the development of atherosclerosis.

Citations

Citations to this article as recorded by  
  • (‐)‐Epicatechin maintains endurance training adaptation in mice after 14 days of detraining
    Maik Hüttemann, Icksoo Lee, Moh H. Malek
    The FASEB Journal.2012; 26(4): 1413.     CrossRef
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The Effect of Sodium Butyrate (SB), Halofuginone Hydrobromide (HH) and High Glucose Concentration on Cell Growth and Gene Expression in Human Aortic Smooth Muscle Cell.
June Ho Park, Sang Jun Lee, Yeo Jun Ki, Young Jung Jeon, Ki Young Kwon, Hong Suk Song, Seung Beom Han, In Kyu Lee, Jung Chul Kim
J Korean Endocr Soc. 2000;15(2):272-285.   Published online January 1, 2001
  • 1,078 View
  • 24 Download
AbstractAbstract PDF
BACKGROUND
Vascular smooth muscle cell (VSMC) proliferation associated with arterial injury causes restenosis, which remains to be resolved in cardiovascular disease, especially after balloon angioplasty. Although numerous factors including hyperglycemia, hyperinsulinemia, angiotensin, basic fibroblast growth factor (BFGF), etc are suggested as potent mitogens for VSMCs, other mechanisms are still needed to take into new consideration. Advances in molecular biology have led to the development of powerful methods for the analysis of differential gene expression. There, we clarified the effect of glucose, sodium butyrate and halofuginon hydrobromide on gene expression which play a role in VSMC growth. METHODS: Therefore, we evaluate the changes of gene expression in response to high glucose concentration, sodium butyrate which is an inhibitor of platelet-derived growth factor (PDGF), and halofuginon hydrobromide which is an inhibitor of specific type 1 collagen, using differntial expressed sequence tag (EST) sequencing and cDNA microarray hybridization. Human mammary artery VSMC isolated from patients undergoing coronary bypass surgery. Cells from passage 3 to 5 were used in experiment with serum-free media with varying conditions. RESULTS: After 6 days of culture, the cells (VSMC) were resuspended with PBS and counted in a hemocytometer, and viable cells were counted using the trypan blue test. VSMC number reached 36?04 cell under high glucose concentration (H/G: 22mM) and 29?04 cell under low glucose concentration(L/G: 5.5 mM) at 6 day of culture (p<0.01). Sodium butyrate(SB) inhibited VSMC growth at varying butyrate concentrations (0.625, 1.25, 2.5, 5.0, 10.0mM) by 84%, 87%, 94%, 96%, 98%, respectively. Halofuginon hydrobromide(HH) also inhibited VSMC growth at varying halofuginon concentrations (10-11, 10-9, 10-7, 10-5mM) by 15%, 30%, 85%, 100%, respectively. Using a differential EST screening technique to assay the relative level of expression of each of large numbers of cloned cDNA sequences after treatment with high glucose concentration (22mM), sodium butyrate (5 mM), and halofuginon (1microM). Among the total 1,730 cDNA clones, 6 cDNA clones were down-regulated after treatment with sodium butyrate (5mM) and halofuginon (1microM). Those were revealed homology to genes encoding connective tissue growth factor (cTGF), Betaig-H3, nm23-H1 nm23-H2, enigma and copine 1. On the contrary, four clones were up-regulated after treatment with high glucose concentration (22mM). Those clones (BO94-5, K1316-5, K1764-5, B1835-5) didn't match any sequence in the public data base. CONCLUSION: These results indicate that this EST analysis is useful technique in targeting genes which are associated with atherosclerosis in VSMC. These identified clones may be used to assist in the positional cloning of genes which are related with atherosclerosis.
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